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• W2083001859 abstract "Prostaglandin E2 (PGE2), interleukin (IL)-23, and IL-1beta (β) propagate inflammatory bowel disease (IBD) by enhancing the development and function of IL-17 producing CD4+ T helper (Th17) cells. CD4+ T cells that express the C-type lectin-like receptor CD161 have been proposed to be the physiologic pool of circulating Th17 cells implicated in IBD. We sought to understand how PGE2, alone and in combination with IL-23 and IL-1β, modulate human peripheral CD161+CD4+ memory T cells. We found that CD161+ cells comprise a significant proportion of human peripheral CD4+ memory T cells. PGE2 and IL-23 plus IL-1β synergistically induced early IL-17A secretion from CD161+CD4+ memory T cells and the selective enrichment of IL-17A+CD161+CD4+ memory T cells in culture. Conversely, IL-23 plus IL-1β partially opposed the PGE2-mediated repression of early interferon gamma (IFN-γ) secretion from CD161+ cells, as well as the PGE2-mediated depletion of IFN-γ+CD161+ cells. Our results suggest that PGE2 and IL-23 plus IL-1β induce the Th17 immune response preferentially in CD161+CD4+ memory T cells, while divergently regulating their ability to express IFN-γ. We hypothesize that Th17-mediated chronic inflammation in IBD depends on the net response of CD161+CD4+ memory T cells to both PGE2 and IL-23 plus IL-1β. Clin Trans Sci 2011; Volume 4: 268–273" @default.
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• W2083001859 date "2011-08-01" @default.
• W2083001859 modified "2023-09-27" @default.
• W2083001859 title "Prostaglandin E2 and IL-23 plus IL-1β Differentially Regulate the Th1/Th17 Immune Response of Human CD161+CD4+ Memory T Cells" @default.
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• W2083001859 doi "https://doi.org/10.1111/j.1752-8062.2011.00300.x" @default.
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